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��ࡱ�>��	�����������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������[�	����bjbj����4�ΐΐ�W�������DD�������������t!$�M(fEKKKK:::�'�'�'�'�'�'�'$�)�U,��']�:::::�'��KK�(fff:��K�K�'f:�'fffK�����YE=3���Rfp'(0M(fE-VE-ff�E-�$&L::f:::::�'�'^:::M(::::��������������������������������������������������������������������E-:::::::::D_:	The fatal ketoacidosis: the diagnostic dilemma in the causes of death in chronic alcohol consumers
Komarekova I, Novomesky F, Janik M, Straka L
Department of Forensic Medicine and Medicolegal Expertises, Jessenius Medical Faculty in Martin, Commenius University in Bratislava






Corresponding author:
Ivana Komarekova, M.D.
Department of Forensic Medicine and Medicolegal Expertises
Kollarova 2
036 01 Martin
Slovakia
ivakomarekova@gmail.com
Summary
Forensic medicine deals with many cases of sudden deaths from various aspects. Above all, the main task for the forensic specialist is to establish the cause of death. It usually becomes clear while based on autopsy, histological, alcoholimetric and toxicological findings. However, in a particular number of cases the cause of death still remains undetermined even after all the procedures mentioned. In up to 10% of sudden or unexpected deaths in patients with anamnesis positive for chronic alcohol intake, the cause and mechanism of death remain unclear even after performing the necropsy (incl. histology) and standard toxicology screening [1, 2]. What is not widely known is that those who chronically and excessively drink alcohol are, like epileptics, at increased risk of sudden death compared to the general population [3]. Commonly, in most of these cases, blood alcohol concentration is low or absent completely and fatty liver is frequently the only pathological abnormal finding detected at the autopsy. These deaths typically occur in white males who are older than 50 years old [4]. We offer a short case report of such a case with the subsequent analysis of why we considered alcoholic ketoacidosis in our differential diagnosis.
Key words: metabolic dysbalance, alcoholic ketoacidosis, chronic alcoholism, sudden death







Introduction
Case report: 
48-years old man was found dead at home, lying in his bed. There was a bucket with liquid vomited remnants with no adiition of fresh or diggested blood found near the bed and an empty bottle of alcalic mineral water often used to attenuate the gastric pain. Up to the information from the man�s relative, he was a chronic alcohol consumer, being last seen alive the day before in the pub, drinking small amount of beer. His personal anamnesis was negative for the previous injuries or any pathological entity which could have potential sudden fatal outcome. External observation of the body did not uncover any signs of mechanical violence on the body. The only pathological findings at the autopsy were: very mild generalised atherosclerosis without stenosis of blood vessels, configuration of the heart with the weight of 400 g was physiological, with no signs of chronic venostatic changes on the internal organs. The microscopical examination did not find any ischemic changes of myocardial muscle. The deceased had diffuse alcoholic steatosis of the liver. The brain was mildly swollen (weight 1300 g) without conformation of conuses and cross section revealed no pathological or traumatic lessions. Results of alcoholimetric analysis were absolutely negative for the presence of ethanol in blood or urine. Toxicological analysis did not notice any psychoactive substances or medicaments, the only finding was positive acetone in blood, level of which was 435 mg/l and highly increased betahydroxybutyric acid (BHBA) blood level of 272 mg/l, while acetonuria was 962 mg/l. Biochemical analysis showed a reduced blood pH=7,21. Sample of vitreous humour showed glucose levels of 3,1 mmol/l.
While analysing the above mentioned case, a few problems arose to be discussed, which were as follows: 
1. Alcohol-related ketoacidosis as a potential �killer�  

Recent and not only forensic studies provide an increasing amount of evidence that rather than being benign, the alcoholic ketoacidosis (AKA) and/or related metabolic disturbances may be a cause of mortality in patients with chronic alcohol dependence [5, 6]. Severe derangements of potassium and/or magnesium ions together with markedly elevated levels of betahydroxybutyric acid (BHBA) may be involved in some of the unexplained sudden deaths of alcoholic patients [1, 7, 8]. AKA is specific BHBA dominated type of ketoacidosis related with enhanced glucagone/insulin and NADH/NAD ratios [9]. In an extent study of cases of sudden deaths in chronic alcoholics, the statistically significant result has been presented, that measured BHBA levels may be even 10 times higher in these cases, than in alcoholic patients in whom another cause of death was found [10]. Denmark [1] noted elevated BHBA levels in a few unexplained deaths and hypothesised that alcohol ketoacidosis may have caused fatal hypoglycaemia which could have lead to death. Thomsen et al  theorised that the acidosis itself causes metabolic disruption of vital functions leading to death, proposing the term �ketoalcoholic death� [7]. Then the authors subsequently reported ketoalcoholic deaths in 7% of sudden deaths in alcoholic patients in a prospective series [8]. Similarly, Pounder et al detected very high levels of total ketone bodies, suggesting profound AKA, in 10% of sudden unexplained deaths in alcoholic patients [11]. Up to these results of previously mentioned international studies, it should be concluded that AKA itself may be a cause of sudden death in severe drinkers due to its direct toxic effects on physiological metabolic pathways.
  

2. The importance of AKA in differential diagnosis 

A reduced blood pH, resulting from the production of beta-oxidative ketone bodies (ketoacidosis) as a result of alcoholism (AKA) or diabetes (diabetic ketoacidosis, DKA), may play the main role in many fatalities. However, in cases of abdominal pains and few vomiting periods, blood pH can vary due to interference with partial metabolic alkalosis after vomiting and respiratory alkalosis caused by severe pain and consequent Kussmaul breathing pattern [12, 13]. Analytical evidence can be used as a dominant support of a pathological diagnosis, or it itself may provide a possible cause of death in the absence of other pathologically significant postmortal findings [14]. 
Therefore AKA must be taken into account in the differential diagnosis of any suddenly deceased alcoholic patient with acidosis, irrespective of the blood glucose concentration [15]. There are relatively few reports of this pathological condition in the literature, but its occurrence may not be infrequent in cases of chronic alcoholism [16]. Although the association between alcohol ingestion and nondiabetic ketoacidosis has been initially speculated for the first time by Dillon in 1940, it has only recently been further documented and studied [17]. The fundamental reason of AKA development in chronic alcohol drinking persons is that they undergo a period of binge drinking, associated with a negligible intake of solid food. After the characteristic development of abdominal pain and severe vomiting - due to pancreatitis, gastritis, or acute hepatitis - the person usually stops drinking. So if the drinker dies subsequently, the presentation of ethanol in blood is frequently undetectable in the sample taken post mortem during the autopsy [14]. The combination of AKA and hypoglycaemic coma in non-diabetic persons has not been described in the literature as a clinical entity, but still it is potentially serious consequence of chronic alcohol intake. Although its treatment is simple and effective, this entity may have a fatal outcome and therefore must be thought of in suddenly deceased chronic alcohol consumers [16].

3. Signs which may lead to diagnosis of AKA
Changes in metabolic processes in patients with alcoholic ketoacidosis are unique. Ketone levels are much higher than those found in normal subjects, even after prolonged fasting [17]. Physiological levels of ketone bodies in blood ranges up to 0,6 mmol/l [18]. On the other hand, the hyperglycemia and glycosuria that accompany severe ketoacidosis in diabetes are absent. Ketosis is part of the physiologic response to carbohydrate deprivation and as such is normally subject of strict and immediate metabolic control [17]. Sex related variations could arise from hormonal and/or nonhormonal mechanisms. Women tend to develop fasting ketonuria and ketonemia more rapidly and more severely than men [19]. Nonhormonal sex differences could also influence the susceptibility to fasting and alcoholic ketoacidosis. The mean postabsorptive free fatty acids (FFA) level in healthy women is significantly higher than in men [19]. These sex differences do not appear to be explained on the basis of differences in age, weight or insulin requirement [20].
4. Diagnostic procedures of AKA available in forensic praxis
The basal problem while testing autopsy blood samples using standard clinical laboratory methods is the postmortal haemolysis. That is why such investigations in forensic praxis should be interpreted cum grano salis only, as to obtain properly interpretable results. Vitreous ketone levels show good correlation with blood and pericardial fluid levels, suggesting that it could be used as an alternative autopsy specimen for the analysis as it can be obtained easily [21]. A gas chromatography-mass spectrometry (GC-MS) for determination of ketone bodies (�-hydroxybutyrate, acetone, and acetoacetate) in blood is the most suitable method.  The ketone bodies in cerebrospinal fluid show the best correlation to blood, while this concentration dependence is mainly due to ketone bodies being utilized by the brain during normal nutritional state. In vitreous humour, the dependence is mainly due to protein bindings of acetoacetate and beta-hydroxybutyrate in blood and the difference in dry matter between blood and vitreous humour [22].
Data from post-mortem blood BHBA, acetone concentrations and vitreous humour glucose concentrations have been collected to determine the markers required to identify and distinguish between AKA, DKA and hyperosmolar hyperglycaemic state (HHS) [11, 14, 21, 22, 23]. Blood BHBA concentrations higher than 250mg/l were considered significant, so it was supposed to be the preferred marker of ketoacidosis [23]. Cases with significant BHBA detected also had the acetone present, demonstrating that the acetone can be used as an initial marker to identify ketoacidosis, thus the acetone can be used to indicate whether BHBA detection is necessary [14]. Vitreous humour glucose concentrations above 6.9mmol/L are considered high and indicative of hyperglycaemia prior to death. Vitreous humour glucose concentrations can be used to distinguish between DKA and ketoacidosis from other causes and to identify deaths due to HHS [23]. 
Additional laboratory tests measuring hormonal and other ketone levels are helpful for recognizing between DKA and AKA. Results of clinical studies of treated and therefore surviving alcohol consuming patients with DKA and AKA disclosed that these two pathological entities differ in their metabolic parameters more than in the hormonal profile. The metabolic profile of DKA is characterized by a higher plasma glucose concentration together with a lower BHBA to acetoacetate and lactate to pyruvate ratios compared with patients with AKA, while the initial hormonal profile in both ketoacidotic states is characterized by similarly decreased insulin levels and elevated levels of counter-regulatory hormones [24, 25].

Conclusion
	The reason why the authors decided to write this article is an experience from their own practise when the diagnostic process of the autopsy itself was not capable of providing the satisfactory cause of death in healthy young individual. Accessory laboratory methods were used to uncover an abnormality in the metabolic status of the deceased, therefore the differential diagnosis of AKA was taken in mind. As proven above, AKA really has irreversible effect on vital functions, if not treated right or on time. Although the human organism did not suffer from any severe disease, it still is very vulnerable to the effects of starving after even a mild alcohol intake. That is why forensic specialists have to use additive laboratory tests combined with the macro- and microscopic findings and fuse them all to a complete puzzle of before separate elements. As in such cases as this one, estimation of ketone bodies may be the only helpful information to rely on in the diagnostic process responsible for concluding the cause of death in young healthy alcohol consumers.




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